Quercetin inhibits inflammatory response induced by lps from porphyromonas gingivalis in human gingival fibroblasts via suppressing nf-b signaling pathway

Abstract

Quercetin, a natural flavonol existing in many food resources, has been reported to be an effective antimicrobial and anti-inflammatory agent for restricting the inflammation in periodontitis. In this study, we aimed to investigate the anti-inflammatory effects of quercetin on Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide-(LPS-) stimulated human gingival fibroblasts (HGFs). HGFs were pretreated with quercetin prior to LPS stimulation. Cell viability was evaluated by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay. The levels of inflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-& (TNF-&), along with chemokine interleukin-8 (IL-8), were determined by enzyme-linked immunosorbent assay (ELISA). The mRNA levels of IL-1β, IL-6, IL-8, TNF-&, IB&, p65 subunit of nuclear factor-kappa B (NF-B), peroxisome proliferator-Activated receptor-γ (PPAR-γ), liver X receptor & (LXR&), and Toll-like receptor 4 (TLR4) were measured by real-Time quantitative PCR (RT-qPCR). The protein levels of IB&, p-IB&, p65, p-p65, PPAR-γ, LXR&, and TLR4 were characterized by Western blotting. Our results demonstrated that quercetin inhibited the LPS-induced production of IL-1β, IL-6, IL-8, and TNF-& in a dose-dependent manner. It also suppressed LPS-induced NF-B activation mediated by TLR4. Moreover, the anti-inflammatory effects of quercetin were reversed by the PPAR-γ antagonist of GW9662. In conclusion, these results suggested that quercetin attenuated the production of IL-1β, IL-6, IL-8, and TNF-& in P. gingivalis LPS-Treated HGFs by activating PPAR-γ which subsequently suppressed the activation of NF-B.